Table of Content

08 August 2018, Volume 45 Issue 8 Previous Issue    Next Issue

For Selected:

Download Citations EndNote Reference Manager ProCite BibTeX RefWorks

Toggle Thumbnails

In vitro expansion of γδT cells and their killing effect on different tumor cells ZHANG Guang-Hui, SHAO Xiao-Yan, YAN Xiao-Min, WEI Shi-Jun 2018, 45 (8):  449-452.  doi: 10.3760/cma.j.issn.1673422X.2018.08.001 Abstract ( 571 )   PDF (2354KB) ( 421 )   Save ObjectiveTo study the killing effect of γδT cells on different tumor cells by inducing and expanding γδT cells in vitro. MethodsCollected the peripheral venous blood of 20 healthy volunteers recruited at Xinqiao Hospital of Third Military Medical University from January to March 2018. Peripheral blood mononuclear cells (PBMCs) were induced and expanded using zoledronic acid combined with interleukin2 (IL2) to obtain γδT cells. The cell purity was detected on day 0, 7, 10, 14 and 16 using flow cytometry. The killing activity was detected by CCK8 kit. Cells cultured on the 14th day were used as effector cells, and breast cancer cell BCap37 and liver cancer cell Bel7402 were used as target cells, and the cell killing activity was detected at the effective target ratio (E∶T) of 5∶1, 10∶1 and 20∶1 respectively. ResultsThe purity of γδT cells were respectively (3.35±1.32)%, (50.76±5.76)%, (80.43±4.53)%, (90.56±3.34)%, (89.54±4.42)% on day 0, 7, 10, 14 , 16, with significant difference (F=18.431, P=0.012). The efficiency of γδT cells killing BCap37 tumor cells were (31.3±2.0)% (E∶T=5∶1), (48.7±1.6)% (E∶T=10∶1), (71.3±2.4)% (E∶T=20∶1) respectively, with significant difference (F=16.724, P=0.016), further comparison between each two groups: 10∶1 vs. 5∶1 (P=0.013), 20∶1 vs. 5∶1 (P=0.017), 20∶1 vs. 10∶1 (P=0.011). The killing rate increased with the increase of target ratio. The efficiency of γδT cells killing Bel7402 tumor cells were (34.5±2.0)% (E∶T=5∶1), (52.4±1.9)% (E∶T=10∶1), (74.5±1.6)% (E∶T=20∶1) respectively, with significant difference (F=18.253, P=0.013), further comparison between each two groups: 10∶1 vs. 5∶1 (P=0.015), 20∶1 vs. 5∶1 (P=0.012), 20∶1 vs. 10∶1 (P=0.015). The killing rate increased with the increase of target ratio. ConclusionWe can obtain high purity γδT cells using zoledronic acid combined with IL2 induced PBMCs, and the amplified γδT cells have significant killing effect on BCap37 and Bel7402 tumor cells. References | Related Articles | Metrics

Effects of osthole on the proliferation, invasion and migration of nasopharyngeal carcinoma cells CNE2 CHEN Jiong-Yu, ZHUANG Yi-Xuan, ZHUANG Shan-Shan, PENG Lin 2018, 45 (8):  453-459.  doi: 10.3760/cma.j.issn.1673422X.2018.08.002 Abstract ( 466 )   PDF (6878KB) ( 342 )   Save ObjectiveTo study the effects of osthole on the proliferation, invasion and migration of nasopharyngeal carcinoma cells CNE2, and to investigate the possible molecular mechanism involved in epithelial to mesenchymal transition (EMT) of CNE2. MethodsCNE2 cells were cultured in vitro and were treated with 0, 20, 40 and 80 μg/ml osthole for 24 or 48 hours, and then methyl thiazolyl tetrazolium (MTT) assay and Transwell assay were used to explore their effects on the cell proliferation, invasion and migration while cells treated with 0 μg/ml osthole were used as the control group. Meanwhile, the mRNA and protein levels of markers of EMT (Ecadherin and vimentin ) and Wnt/βcatenin signaling (βcatenin and cyclin D1) were detected by reverse transcriptionpolymerase chain reaction (RTPCR) and Western blotting respectively. ResultsAfter treatment for 24 and 48 hours, the inhibitory rates of treatment with various concentration of osthole (0, 20, 40, 80 μg/ml) were 0.00%±0.00%, 7.45%±0.87%, 14.12%±2.29%, 27.26%±0.43% and 0.00%±0.00%, 13.44%±0.84%, 29.03%±0.78%, 57.49%±1.70%, with significant differences (F=174.33, P<0.001; F=1 041.40, P<0.001), and the following contrast between each two groups met the statistical significance (all P＜0.01). The migration cells per field of CNE2 cells treated with 0, 20, 40, 80 μg/ml osthole for 48 hours were 52.13±4.49, 29.00±4.49, 18.50±1.93, 13.75±2.77, which exhibited a significant difference (F=200.37, P＜0.001), and the following contrast between each two groups met the statistical significance (all P＜0.01). The invasion cells per field of CNE2 cells treated with 0, 20, 40, 80 μg/ml osthole for 48 hours were 46.63±2.87, 24.13±2.87, 16.75±5.29, 11.00±1.77 respectively, which exhibited a significant difference (F=131.92, P＜0.001), and the following contrast between each two groups met the statistical significance (all P＜0.01). Meanwhile, the relative mRNA and protein expressions of Ecadherin in 0, 20, 40 and 80 μg/ml osthole treatedcells (exposure for 48 hours) were 1.00±0.13, 2.61±0.03, 3.12±0.09, 3.60±0.06 (F=20.92, P<0.001) and 0.22±0.03, 0.35±0.01, 0.60±0.04, 0.82±0.03 (F=178.63, P＜0.001) respectively, and the differences were statistically significant, and further pairwise comparison showed the differences were statistically significant (all P＜0.05). Furthermore, the relative mRNA and protein levels of vimentin, βcatenin, cyclin D1 in 0, 20, 40 and 80 μg/ml osthole treatment for 48 hours were statistically significant difference (mRNA level of vimentin: 1.00±0.12, 0.68±0.03, 0.56±0.01, 0.40±0.09, F=9.48, P<0.010; mRNA level of βcatenin: 1.00±0.14, 0.78±0.04, 0.69±0.07, 0.46±0.12, F=4.84, P<0.050; mRNA level of cyclin D1: 1.00±0.09, 0.82±0.03, 0.58±0.09, 0.40±0.03, F=9.49, P<0.010; protein level of vimentin: 0.85±0.02, 0.74±0.01, 0.34±0.01, 0.27±0.01, F=610.58, P<0.001; protein level of βcatenin: 0.83±0.00, 0.44±0.02, 0.39±0.00, 0.23±0.03, F=985.74, P＜0.001; protein level of cyclin D1: 0.86±0.02, 0.67±0.00, 0.35±0.01, 0.25±0.01, F=910.57, P＜0.001), and further pairwise comparison showed the differences were statistically significant (all P＜0.05). ConclusionOsthole can inhibit the proliferation, invasion and migration of CNE2 cells, which is related to the regulation of Wnt/βcatenin signal pathway and then suppressing of EMT. Related Articles | Metrics

Expression and clinical significance of serum microRNA663 in nasopharyngeal carcinoma patients LAI Shi-Jia, ZHAO De-An, SUN Yong-Ming 2018, 45 (8):  460-464.  doi: 10.3760/cma.j.issn.1673422X.2018.08.003 Abstract ( 418 )   PDF (2344KB) ( 413 )   Save ObjectiveTo investigate the expression level of serum microRNA663 (miR663) in nasopharyngeal carcinoma (NPC) patients and its relationships with clinicopathological features and prognosis. MethodsThe serums of 60 NPC patients (NPC group), 40 patients with nasopharyngeal chronic inflammation (nasopharyngitis group) and 30 healthy subjects (health control group) were collected from June 2014 to April 2017 in our hospital. The relative expression levels of serum miR663 were detected by quantitative real time polymerase chain reaction (qRTPCR). The relationships between the expression of miR663 and clinicopathological features were analyzed. The diagnostic value of serum miR663 in patients with NPC was analyzed by receiver operating characteristic (ROC) curve. According to the optimal cutoff value determined by the ROC curve, the patients were divided into miR663≥optimal cutoff value group and miR663<optimal cutoff value group, and prognosis analysis was performed for the two groups. ResultsThe relative expression levels of miR663 among NPC group (6.38±2.05), nasopharyngitis group (3.11±0.97) and health control group(1.74±0.75) were significantly different (F=107.722, P=0.001). Serum miR663 level in NPC group was significantly higher than that in nasopharyngitis group and healthy control group, with significant differences (both P＜0.001). The relative expression level of miR663 in nasopharyngitis group was significantly higher than that in health control group, with a significant difference (P＜0.001). The relative expression of serum miR663 in patients with NPC was not related to patient′s age, sex and differentiation (t=1.832, P=0.072; t=0.578, P=0.565; F=0.132, P=0.877). The relative expression of miR663 in stage ⅠⅡ (5.24±1.98) was significantly lower than that in stage ⅢⅣ (6.99±1.84) of NPC patients, with a significant difference (t=3.417, P＜0.001). The relative expression of serum miR663 in patients with lymph node metastasis (7.55±1.38) was significantly higher than that in patients without lymph node metastasis (4.62±1.60), with a significant difference (t=7.572, P=0.001). The analysis of the diagnostic value of serum miR663 in patients with NPC using the ROC curve showed that the area under the curve (AUC) of miR663 was 0.939. When the optimal cutoff value of miR663 was 3.190, the sensitivity was 80.0% and the specificity was 89.0%. The median survival time in miR663≥3.190 group (21.7 months) was significantly shorter than that in miR663＜3.190 group (33.4 months), with a significant difference (χ2=4.332, P=0.037). ConclusionThe relative expression level of serum miR663 in patients with NPC is increased, and the expression level of miR663 is related to lymph node metastasis and clinical stage. High expression of miR663 predicts poor clinical outcomes, and miR663 may be a potential predictor of prognosis in patients with NPC. References | Related Articles | Metrics

Relationship between serum ferritin, erythrocyte sedimentation rate, mean corpuscular indexes and prognosis in patients with small cell lung cancer XIE Jin-Hua, JI Hao-Ming, CHEN Guo-Dong, WANG Yu, SHEN Yu-Cheng 2018, 45 (8):  465-469.  doi: 10.3760/cma.j.issn.1673422X.2018.08.004 Abstract ( 889 )   PDF (2294KB) ( 525 )   Save ObjectiveTo explore the clinical value of serum ferritin (SF), erythrocyte sedimentation rate (ESR) and erythrocyte average indexes ［mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC)］ in the prognosis evaluation of patients with small cell lung cancer (SCLC). MethodsA total of 72 SCLC patients were enrolled in the Haian People′s Hospital Affiliated to Nantong University from January 2013 to October 2016 (SCLC group), and 80 health controls were selected at the same time (control group). The levels of serum SF, ESR and erythrocyte average indexes in SCLC group and control group were detected, and their relationships with clinical features, prognosis and survival time were analyzed. ResultsThe serum levels of SF, ESR, MCV, MCH and MCHC in SCLC patients were (309±59) μg/L, (16±4) mm/h, (104±12) fl, (32±4) pg and (307±21) g/L, respectively. The serum levels of SF, ESR, MCV, MCH and MCHC in control group were (186±26) μg/L, (15±5) mm/h, (85±7) fl, (30±3) pg and (335±25) g/L, respectively. Compared with the control group, the patients in SCLC group were significantly increased on the levels of SF (t=14.168, P<0.001) and MCV (t=6.143, P<0.001), and were significantly decreased on the level of MCHC (t=-4.220, P=0.003). There were no significant difference in the levels of ESR (t=1.931, P=0.102) and MCH (t=1.220, P=0.313) between the two groups. The serum levels of SF and MCV were significantly correlated with the stage of SCLC (t=-4.092, P=0.009; t=-4.985, P<0.001). Multivariate logistic regression analysis showed that high serum SF (OR=5.31, 95%CI: 3.099.31, P<0.001) and MCV (OR=1.78, 95%CI: 1.103.08, P=0.013) were independent risk factors of SCLC. Survival analysis showed that the survival time of the patients in the high SF group was significantly shorter than that in the low SF group (6 months vs. 20 months; χ2=6.556, P=0.001). ConclusionSerum ESR, MCH and MCHC levels are not significantly correlated with SCLC, but serum SF and MCV levels are of important clinical significance in evaluating the prognosis of SCLC patients. References | Related Articles | Metrics

Effect of miR145 targeting Six1 on invasion of gastric cancer and its molecular mechanism JIANG Li, LI Hui, ZHANG Gui-Ying, MU Yi-Bing, LIU Hai-Tao 2018, 45 (8):  470-477.  doi: 10.3760/cma.j.issn.1673422X.2018.08.005 Abstract ( 540 )   PDF (6574KB) ( 296 )   Save ObjectiveTo investigate the expressions of microRNA145 (miR145) and Six1 in gastric cancer tissues and gastric cancer cell lines, and to investigate the effect of miR145 targeting Six1 on invasion of human gastric cancer cells and its molecular mechanism. MethodsSixty patients with advanced gastric cancer confirmed by gastroscopy and pathology in the Fourth Hospital of Changsha were selected, from January to November, 2017. The expressions of miR145 mRNA and Six1 in 60 cases of gastric cancer and their matched adjacent tissues were detected by realtime fluorescence quantitative PCR (qRTPCR) and their correlations were analyzed. miR145 mimics were transfected into MKN45, BGC823 and SGC7901 gastric cancer cell lines. The relative levels of miR145 mRNA in three gastric cancer cell lines were detected by qRTPCR. The SGC7901 gastric cancer cell lines with the highest expression level of miR145 mRNA were selected for subsequent experiments. The mimic group (transfected with miR145 mimic), NC group (transfected with miR145 negative control) and empty carrier group (no addition of any oligonucleotides) were set up. The invasive ability of gastric cancer cells was detected by Transwell test. The ability of angiogenesis was verified by microtubule formation experiment. The expression levels of downstream proteins of the gastric cancer cell lines SGC7901 such as Six1, Ecadherin and vimentin were detected by Western blotting method. The MirTrap system and the luciferase report test verified whether miR145 targeted the Six1 gene. ResultsThe expressions of miR145 mRNA in gastric cancer tissues and in para cancerous tissues were 0.579±0.086 and 1.009±0.121, respectively. The difference was statistically significant (t=-22.498, P<0.001). The expressions of Six1 were 2.516±0.208 and 1.041±0.227, respectively. The difference was statistically significant (t=37.119, P<0.001). The expressions of miR145 mRNA and Six1 were negatively correlated (r=－0.728, P<0.001). After overexpression of miR145, in the mimic, NC and empty carrier groups, the numbers of cells passing through the membrane were 48.550±3.716, 82.800±3.797, 87.467±8.023, respectively. The difference was statistically significant (F=87.789, P<0.001). There were significant differences between the mimic and NC groups and between the mimic and empty carrier groups (both P<0.001). In the mimic, NC and empty carrier groups, the numbers of tube formation of human umbilical vein endothelial cells were 24.333±1.211, 34.167±2.041, 36.500±3.209, respectively. The difference was statistically significant (F=47.103, P<0.001). There were significant differences between the mimic and NC groups and between the mimic and empty carrier groups (both P<0.001). In the mimic, NC and empty carrier groups, the expression levels of Six1 in gastric cancer SGC7901 cells were 1.392±0.072, 2.426±0.099, 2.371±0.079, respectively. The difference was statistically significant (F=289.517, P<0.001). There were significant differences between the mimic and NC groups and between the mimic and empty carrier groups (both P<0.001). In the mimic, NC and empty carrier groups, the expression levels of Ecadherin were 4.001±0.132, 2.714±0.181, 2.653±0.218, respectively. The difference was statistically significant (F=106.572, P<0.001). There were significant differences between the mimic and NC groups and between the mimic and empty carrier groups (both P<0.001). In the mimic, NC and empty carrier groups, the expression levels of vimentin were 1.634±0.132, 3.349±0.102, 3.501±0.185, respectively. The difference was statistically significant (F=389.032, P<0.001). There were significant differences between the mimic and NC groups and between the mimic and empty carrier groups (both P<0.001). MirTrap system verified that the target Six1 mRNA levels in the mimic, NC and empty carrier groups were 1.101±0.097, 0.582±0.037, 0.573±0.032, respectively. The difference was statistically significant (F=138.922, P<0.001). There were significant differences between the mimic and NC groups and between the mimic and empty carrier groups (both P<0.001). Luciferase reporter assay showed that the double fluorescence ratios of Six1 wild type recombinant vector group were 7.324±0.415, 10.755±0.481, 10.430±0.309 in the mimic, NC and empty carrier groups respectively. The difference was statistically significant (F=129.345, P<0.001). There were significant differences between the mimic and NC groups and between the mimic and empty carrier groups (both P<0.001). The double fluorescence ratios of Six1 mutant recombinant vector group were 10.938±0.091, 11.077±0.126, 11.028±0.205 in the mimic, NC and empty carrier groups respectively, and the difference was not statistically significant (F=1.318, P=0.297). The MirTrap system and the luciferase report test showed that miR145 was targeted to the Six1 gene. ConclusionThe expressions of miR145 mRNA and Six1 in gastric cancer and para cancerous tissues were different and negatively correlated. miR145 inhibited the invasion, angiogenesis and epithelial mesenchymal transition of gastric cancer cells by targeting Six1 gene. References | Related Articles | Metrics

Relationships between expression of hypoxiainducible factor1α protein and clinicopathological characteristics and prognosis of patients with gastric cancer HUANG Chun-Zhen, LI Jian-Wang, YUAN Jian-Hua, MAO Shan-Shan, CHEN Qiong-Hui, ZHANG Wei-Fang 2018, 45 (8):  478-482.  doi: 10.3760/cma.j.issn.1673422X.2018.08.006 Abstract ( 440 )   PDF (2303KB) ( 470 )   Save ObjectiveTo investigate the expression level of hypoxiainducible factor1α (HIF1α) in gastric cancer and its relationship with clinicopathological characteristics and prognosis of patients with gastric cancer. MethodsFrom March 3, 2011 to September 28, 2012, 49 patients with gastric adenocarcinoma tissue chips were selected from pathology department of our hospital. They were matched with paracancerous tissues. The expression levels of HIF1α were measured by immunohistochemistry method in gastric cancer tissues and paracancerous tissues chips. KaplanMeier was used to evaluate the progressionfree survival (PFS) and overall survival (OS), and the Cox proportional hazards model was used to analyze whether HIF1α was a prognostic factor. ResultsThe high expression rate of HIF1α protein in gastric cancer was significantly higher than that in paired paracarcinoma group (42.9% vs. 4.1%, χ2=20.509, P<0.001). The expression of HIF1α protein was related to TNM stage (χ2=4.601, P=0.032), vascular invasion (χ2=6.766, P=0.009) and degree of differentiation (χ2=7.969, P=0.005). Compared with patients with low expression of HIF1α, the median PFS (16.2 months vs. 27.3 months) and median OS (34.8 months vs. 43.8 months) were shorter in the patients with high expression of HIF1α, and the differences were statistically significant (median PFS: χ2=4.661, P=0.002; median OS: χ2=6.903, P=0.009). The results of single factor analysis showed that overexpression of HIF1α was correlated with PFS and OS (PFS: HR=4.461, 95%CI: 1.96910.802, P＜0.001; OS: HR=3.109, 95%CI: 1.2747.588,P=0.013).  The results of Cox multivariate analysis showed that overexpression of HIF1α was the independent risk factor that affected the survival and prognosis of patients with gastric cancer (PFS: HR=4.747, 95%CI: 2.17510.230, P＜0.001; OS: HR=3.171, 95%CI: 1.3587.404, P=0.008). ConclusionThe high expression rate of HIF1α protein in gastric cancer tissues is significantly higher than that in paracancerous tissues. The expression of HIF1α is associated with TNM stage, vascular invasion, degree of differentiation in patients with gastric cancer. The high expression of HIF1α is associated with the shorter median OS and PFS. The high expression of HIF1α is an independent risk factor for the survival and prognosis of patients with gastric cancer, which is expected to be an independent marker of poor prognosis. Related Articles | Metrics

Expression of CIAPIN1 protein in colon cancer and its relationship with pathological features of tumor YUAN Yang-Jun, LU Da-Song, DENG Bing-Qu 2018, 45 (8):  483-486.  doi: 10.3760/cma.j.issn.1673422X.2018.08.007 Abstract ( 494 )   PDF (2053KB) ( 415 )   Save ObjectiveTo investigate the expression of cytokine induced apoptosis inhibitor 1 (CIAPIN1) protein in colon cancer tissues and its relationship with the pathological features of tumor. MethodsA total of 80 cases of colon cancer tissues and 40 cases of paracancer tissues were collected from our hospital after surgery from January 2014 to January 2017. Immunohistochemical staining and Western blotting were used to detect the expressions of CIAPIN1 protein in the two types of specimens. The relationships between CIAPIN1 protein and the occurrence and development of colon cancer were analyzed. ResultsThe positive rate of CIAPIN1 protein expression in colon cancer tissues was significantly lower than that in paracancer tissues (30.0% vs. 85.0%, χ2=32.303, P<0.001). The relative expression level of CIAPIN1 protein in colon cancer tissues was significantly lower than that in paracancer tissues (0.507±0.183 vs. 1.874±0.361, t=22.513, P<0.001). The positive expression rate of CIAPIN1 in colon cancer tissues was not correlated with the age (χ2=0.086, P=0.769), sex (χ2=0.779, P=0.377), tumor invasion depth (χ2=0.879, P=0.348), tumor location (χ2=0.725, P=0.395), tumor size (χ2=2.241, P=0.134), tumor differentiation status(χ2=1.372, P=0.241), and the pathological type (P=0.715), but was significantly correlated with lymph node metastasis (χ2=10.813, P=0.001) and clinical stage (χ2=5.610, P=0.018). ConclusionThe expression of CIAPIN1 protein in colon cancer tissues reduces significantly, and is correlated with clinical stage and lymph node metastasis. References | Related Articles | Metrics

Immunological regulation of CD70/CD27 pathway and the expression of CD70 in tumor LIU Zhen-Zhen, KONG Ying-Jun, SUN Wen-Xue, LI Shi-Min, ZHANG Min, YIN He-Song 2018, 45 (8):  487-489.  doi: 10.3760/cma.j.issn.1673422X.2018.08.008 Abstract ( 671 )   PDF (1726KB) ( 456 )   Save CD70/CD27 pathway plays an important role in human immune regulation. The role of CD70/CD27 pathway in immune regulation is mainly to promote the activation and proliferation of T cells, induce the differentiation and formation of effector T cells and memory T cells, and interfere with regulatory T cells. In addition, the high level of CD70 expression in some tumor cells provides a new way for tumor immunotherapy. Related Articles | Metrics

Antitumor therapy of thalidomide WU Xin, QU Xiu-Juan, ZHANG Ling-Yun 2018, 45 (8):  490-493.  doi: 10.3760/cma.j.issn.1673422X.2018.08.009 Abstract ( 1330 )   PDF (1605KB) ( 547 )   Save Studies have found that thalidomide has antitumor activity due to its inhibitory effect on angiogenesis and immunomodulation, which has been effectively used in targeted therapy resistant nonsmall cell lung cancer, castrationresistant prostate cancer, colorectal cancer, advanced hepatocarcinoma and advanced gastric cancer. Many clinical studies have also found that it has certain practical value in the aspects of improvement of cancer cachexia and chemotherapyinduced nausea and vomiting. Related Articles | Metrics

Molecular mechanism in malignant progression of meningioma LIU Hou-Jie, WAN Jing-Hai 2018, 45 (8):  494-498.  doi: 10.3760/cma.j.issn.1673422X.2018.08.010 Abstract ( 605 )   PDF (3069KB) ( 556 )   Save Atypical and malignant meningiomas are characterized by high invasiveness and local recurrence. Traditional treatments such as surgery, radiotherapy and chemotherapy have limited effects. Recently, with the further study of the pathogenesis of meningioma and the development of molecular biology techniques, some new biomarkers have been found to play important roles in development and malignant progression of meningioma. Several genetic and epigenetic factors have been identified as contributing to the malignant progression of meningioma. Genetic factors include multiple phenotypic changes such as abnormal cell proliferation, increased cell invasiveness, angiogenesis, apoptosis inhibition, and changes in telomerase activity. And the discovery of biomarkers provides references for early diagnosis, molecular targeted therapy and prognosis assessment of highgrade meningiomas. Related Articles | Metrics

Application of volumetric modulated arc therapy in esophageal cancer HE Xiao-Lan, XU Xiao-Ting 2018, 45 (8):  499-501.  doi: 10.3760/cma.j.issn.1673422X.2018.08.011 Abstract ( 526 )   PDF (1741KB) ( 415 )   Save Esophageal cancer is a common gastrointestinal tumor in China with high morbidity and mortality. As a new radiotherapy technique, volumetric modulated arc therapy (VMAT) is increasingly used for the treatment of esophageal cancer. VMAT can reduce the dose of endanger organs, protect the organs and reduce the side effects of radiotherapy. For esophageal cancer patients with different location and volume, VMAT can effectively improve the safety and efficiency of treatment by reducing the treatment time and improving the conformability of the target area. Combined with chemotherapy before operation, VMAT increases the chance of tumor reduction, and improves the success rate of operation. Besides, studies have shown that increasing the number of VMAT programs can improve the accuracy of target area and reduce the time of treatment. VMAT has become an important way to treat patients with esophageal cancer.   Related Articles | Metrics

Current status and prospects of immunotherapy in esophageal cancer YU Xiao-Qing, FAN Yun 2018, 45 (8):  502-505.  doi: 10.3760/cma.j.issn.1673422X.2018.08.012 Abstract ( 715 )   PDF (2327KB) ( 584 )   Save The treatment of esophageal cancer is difficult in clinic. Recently, the development of immune checkpoint inhibitors has brought the immunotherapies to a new age. In predicting the curative effect of biomarkers, programmed cell deathligand 1, tumor mutation burden and microsatellite instability could promisingly predict the effect of the immune checkpoint inhibitors. Various immune checkpoint inhibitors are emerging and the combination of immunotherapy have shown a great applied potential in a series of clinical trials of esophageal cancer.  Related Articles | Metrics

Molecular mechanisms of castrationresistant prostate cancer progressed from prostate cancer by androgen deprivation treatment XU Yao-Zong, GU Xiao, WANG Fei, DING Xue-Fei 2018, 45 (8):  506-509.  doi: 10.3760/cma.j.issn.1673422X.2018.08.013 Abstract ( 582 )   PDF (2317KB) ( 571 )   Save ［1］ Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016［J］. CA Cancer J Clin, 2016, 66(1): 730. DOI: 10.3322/caac.21332. ［2］  Chen W, Zheng R, Baade PD, et al. Cancer statistics in China, 2015［J］. CA Cancer J Clin, 2016, 66(2): 115132. DOI: 10.3322/caac.21338. ［3］  Heidenreich A, Bastian PJ, Bellmunt J, et al. EAU guidelines on prostate cancer. Part Ⅱ: treatment of advanced, relapsing, and castrationresistant prostate cancer［J］. Eur Urol, 2014, 65(2): 467479. DOI: 10.1016/j.eururo.2013.11.002. ［4］ Cornford P, Bellmunt J, Bolla M, et al. EAUESTROSIOG guidelines on prostate cancer. Part Ⅱ: treatment of relapsing, metastatic, and castrationresistant prostate cancer［J］. Eur Urol, 2017, 71(4): 630642. DOI: 10.1016/j.eururo.2016.08.002. ［5］ Ceder Y, Bjartell A, Culig Z, et al. The molecular evolution of castrationresistant prostate cancer［J］. Eur Urol Focus, 2016, 2(5): 506513. DOI: 10.1016/j.euf.2016.11.012. ［6］ Chandrasekar T, Yang JC, Gao AC, et al. Mechanisms of resistance in castrationresistant prostate cancer (CRPC)［J］. Transl Androl Urol, 2015, 4(3): 365380. DOI: 10.3978/j.issn.22234683.2015.05.02. ［7］ Yamamoto Y, Loriot Y, Beraldi E, et al. Generation 2.5 antisense oligonucleotides targeting the androgen receptor and its splice variants suppress enzalutamideresistant prostate cancer cell growth［J］. Clin Cancer Res, 2015, 21(7): 16751687. DOI: 10.1158/10780432.CCR141108. ［8］ Mostaghel EA, Marck BT, Plymate SR, et al. Resistance to CYP17A1 inhibition with abiraterone in castrationresistant prostate cancer: induction of steroidogenesis and androgen receptor splice variants［J］. Clin Cancer Res, 2011, 17(18): 59135925. DOI: 10.1158/10780432.CCR110728. ［9］ Romanel A, Gasi Tandefelt D, Conteduca V, et al. Plasma AR and abirateroneresistant prostate cancer［J］. Sci Transl Med, 2015, 7(312): 312re10. DOI: 10.1126/scitranslmed.aac9511. ［10］  Boudadi K, Antonarakis ES. Resistance to novel antiandrogen therapies in metastatic castrationresistant prostate cancer［J］. Clin Med Insights Oncol, 2016, 10(Suppl1): 19. DOI: 10.4137/CMO.S34534. ［11］ Korpal M, Korn JM, Gao X, et al. An F876L mutation in androgen receptor confers genetic and phenotypic resistance to MDV3100 (enzalutamide)［J］. Cancer Discov, 2013, 3(9): 10301043. DOI: 10.1158/21598290.CD130142. ［12］ Kong D, Sethi S, Li Y, et al. Androgen receptor splice variants contribute to prostate cancer aggressiveness through induction of EMT and expression of stem cell marker genes［J］. Prostate, 2015, 75(2): 161174. DOI: 10.1002/pros.22901. ［13］ Jin R, Yamashita H, Yu X, et al. Inhibition of NFkappa B signaling restores responsiveness of castrateresistant prostate cancer cells to antiandrogen treatment by decreasing androgen receptor variants expression［J］. Oncogene, 2015, 34(28): 37003710. DOI: 10.1038/onc.2014.302. ［14］ Deng C, Chen J, Guo S, et al. CX4945 suppresses the growth of castrationresistant prostate cancer cells by reducing ARV7 expression［J］. World J Urol, 2017, 35(8): 12131221. DOI: 10.1007/s003450161996y. ［15］ Ryan CJ, Smith MR, Fizazi K, et al. Abiraterone acetate plus prednisone versus placebo plus prednisone in chemotherapynaive men with metastatic castrationresistant prostate cancer (COUAA302): final overall survival analysis of a randomised, doubleblind, placebocontrolled phase 3 study［J］. Lancet Oncol, 2015, 16(2): 152160. DOI: 10.1016/S14702045(14)712057. ［16］ Shi XB, Xue L, Ma AH, et al. Tumor suppressive miR124 targets androgen receptor and inhibits proliferation of prostate cancer cells［J］. Oncogene, 2013, 32(35): 41304138. DOI: 10.1038/onc.2012.425. ［17］ Wan X, Huang W, Yang S, et al. Androgeninduced miR27A acted as a tumor suppressor by targeting MAP2K4 and mediated prostate cancer progression［J］. Int J Biochem Cell Biol, 2016, 79: 249260. DOI: 10.1016/j.biocel.2016.08.043. ［18］ Wan X, Pu H, Huang W, et al. Androgeninduced miR135a acts as a tumor suppressor through downregulating RBAK and MMP11, and mediates resistance to androgen deprivation therapy［J］. Oncotarget, 2016, 7(32): 5128451300. DOI: 10.18632/oncotarget.9992. ［19］ Carver BS. Defining and targeting the oncogenic drivers of neuroendocrine prostate cancer［J］. Cancer Cell, 2016, 29(4): 431432. DOI: 10.1016/j.ccell.2016.03.023. ［20］ Tan HL, Sood A, Rahimi HA, et al. Rb loss is characteristic of prostatic small cell neuroendocrine carcinoma［J］. Clin Cancer Res, 2014, 20(4): 890903. DOI: 10.1158/10780432.CCR131982. ［21］ Ku SY, Rosario S, Wang Y, et al. Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance［J］. Science, 2017, 355(6320): 7883. DOI: 10.1126/science.aah4199. ［22］ Mu P, Zhang Z, Benelli M, et al. SOX2 promotes lineage plasticity and antiandrogen resistance in TP53 and RB1deficient prostate cancer［J］. Science, 2017, 355(6320): 8488. DOI: 10.1126/science.aah4307. ［23］ Dang Q, Li L, Xie H, et al. Antiandrogen enzalutamide enhances prostate cancer neuroendocrine (NE) differentiation via altering the infiltrated mast cells→androgen receptor (AR)→miRNA32 signals［J］. Mol Oncol, 2015, 9(7): 12411251. DOI: 10.1016/j.molonc.2015.02.010. ［24］ Shiota M, Yokomizo A, Takeuchi A, et al. Inhibition of protein kinase C/Twist1 signaling augments anticancer effects of androgen deprivation and enzalutamide in prostate cancer［J］. Clin Cancer Res, 2014, 20(4): 951961. DOI: 10.1158/10780432.CCR131809. ［25］ Shang Z, Cai Q, Zhang M, et al. A switch from CD44+ cell to EMT cell drives the metastasis of prostate cancer［J］. Oncotarget, 2015, 6(2): 12021216. DOI: 10.18632/oncotarget.2841. ［26］ Leong KG, Wang BE, Johnson L, et al. Generation of a prostate from a single adult stem cell［J］. Nature, 2008, 456(7223): 804808. DOI: 10.1038/nature07427. ［27］ Jain AK, Allton K, Iacovino M, et al. p53 regulates cell cycle and microRNAs to promote differentiation of human embryonic stem cells［J］. PLoS Biol, 2012, 10(2): e1001268. DOI: 10.1371/journal.pbio.1001268. ［28］ Li L, Dang Q, Xie H, et al. Infiltrating mast cells enhance prostate cancer invasion via altering LncRNAHOTAIR/PRC2androgen receptor (AR)MMP9 signals and increased stem/progenitor cell population［J］. Oncotarget, 2015, 6(16): 1417914190. DOI: 10.18632/oncotarget.3651. ［29］ Akamatsu, Wyatt AW, Lin D, et al. The placental gene PEG10 promotes progression of neuroendocrine prostate cancer［J］. Cell Rep, 2015, 12(6): 922936. DOI: 10.1016/j.celrep.2015.07.012. Related Articles | Metrics